Leprosy has a fixed place in the standard history of the Americas: one of the diseases Europeans brought after 1492, alongside smallpox and measles. That account rested on the assumption that leprosy means Mycobacterium leprae, the pathogen documented across medieval Europe and Asia — and on the absence of convincing pre-contact skeletal evidence.
A 2025 study takes that apart. It shows that a second leprosy-causing bacterium, Mycobacterium lepromatosis, was infecting people in the Americas before European contact, with ancient genomes recovered from individuals in Canada and Argentina dating to roughly a thousand years ago.
The evidence comes from Pre-European contact leprosy in the Americas and its current persistence in Science, which screened 389 ancient and 408 contemporary samples.
The short answer: M. lepromatosis, a leprosy pathogen distinct from M. leprae and found mainly in the Americas, infected people there before European arrival. Ancient genomes from Canada and Argentina — thousands of kilometres apart, from similar periods — are genetically close, suggesting the bacterium was widespread during the Late Holocene. Phylogenetic analysis also identifies distinct human-infecting clades, one of which has dominated North America since colonial times.
Two bacteria, one disease name#
"Leprosy" names a clinical picture — chronic infection producing skin lesions and nerve damage — rather than a single organism. For most of the history of the disease's study, only one cause was known.
M. lepromatosis was described as a separate species only in 2008, from a pair of Mexican patients with an unusually severe presentation. It is genetically distinct from M. leprae, having diverged from it a very long time ago, and its known distribution is unlike M. leprae's: it is found chiefly in the Americas, and it has been detected in red squirrels in the British Isles.
That distribution was the loose thread. A leprosy pathogen concentrated in the Americas raises an obvious question about how long it had been there — and the assumption that leprosy arrived with Europeans had been formed when nobody knew this species existed.
| M. leprae | M. lepromatosis | |
|---|---|---|
| Described | 1873 | 2008 |
| Main distribution | Global, historically dense in Europe and Asia | Mainly the Americas |
| Non-human hosts | Armadillos, chimpanzees | Red squirrels (British Isles) |
| Role in the standard narrative | The pathogen assumed to have been introduced after 1492 | Absent from the narrative entirely |
Screening at scale#
The study's design is the reason it could answer the question. Rather than testing a handful of skeletons with visible lesions, the team screened 389 ancient samples alongside 408 contemporary ones, substantially expanding the genetic data available for a species that had barely been sequenced.
That matters because of how palaeopathology usually works. Leprosy is diagnosed in skeletons from characteristic bone changes — but those changes take years to develop, appear in only a fraction of cases, and can be mimicked by other conditions. Screening by DNA rather than by lesion removes the requirement that the disease had progressed far enough to reshape bone, and removes the circularity of only testing individuals who already look like cases.
From that screen came ancient M. lepromatosis genomes from Canada and Argentina, both from contexts predating European contact, and both dating to roughly a thousand years ago.
Two continents, one close pair of strains#
The most informative result is the relationship between the two ancient genomes. The Canadian and Argentinian individuals lived several thousand kilometres apart, at opposite ends of two continents, and the strains they carried are genetically close.
A pathogen that had entered the Americas recently and spread slowly would not produce that pattern; strains at either end of the hemisphere would be expected to have diverged substantially. Close relatives at that distance imply either widespread circulation with ongoing connection, or a relatively recent expansion of the lineage across an already-occupied range.
Either reading supports the paper's conclusion: M. lepromatosis was likely widespread during the Late Holocene, not a local curiosity in one region.
The phylogenetic analysis adds a second layer. It resolves distinct human-infecting clades, one of which has dominated North America since colonial times — meaning the modern picture is not simply the ancient one continued. Something changed around and after contact, favouring one lineage over the others.
What the study does not claim#
Three misreadings are easy here, and worth heading off.
It does not say leprosy was common. Two ancient genomes from two individuals establish presence, not prevalence. How many people were infected, in what regions, at what rates — none of that follows.
It does not say M. leprae was present too. The pre-contact evidence concerns M. lepromatosis specifically. The introduction of M. leprae to the Americas during and after colonisation is not challenged by this work.
It does not reframe the epidemiological catastrophe of contact. The mass mortality that followed European arrival was driven by acute epidemic diseases against which Indigenous populations had no prior exposure. Leprosy is a chronic, low-transmissibility infection with a years-long incubation; its presence beforehand does not alter that history in any way.
What the study does establish is narrower and still significant: one component of the "diseases Europeans brought" list was there already, and was missed because nobody was looking for a species that had not yet been named.
Why pathogen genomics keeps rewriting these stories#
This result belongs to a pattern. Ancient DNA has repeatedly found pathogens earlier, and in places, that the received history did not allow — plague among Siberian hunter-gatherers 5,500 years ago being a close parallel, since it too overturned an assumption about the social conditions a disease supposedly required.
The mechanism behind the pattern is consistent. Historical disease narratives were built from written records and from skeletal lesions, and both are biased in the same direction: they see diseases that were noticed and named, in populations that produced documents, in cases advanced enough to mark bone. A screening programme that tests hundreds of samples for pathogen DNA regardless of appearance has none of those filters.
It is a reminder that "there is no evidence for X" in palaeopathology has often meant "nobody has tested for X" — a distinction that matters most for regions and periods whose histories were written by outsiders.
What changed after 1492#
The phylogenetic result about distinct human-infecting clades, one of which has dominated North America since colonial times, deserves separate attention, because it describes a change rather than a continuity.
If the pre-contact bacterium had simply persisted, the modern North American picture would be expected to preserve the diversity that existed beforehand. Instead one lineage came to predominate. That is the shape produced when a population passes through a bottleneck, or when one variant expands into space that others previously occupied.
The plausible drivers are not mysterious. The colonial period devastated Indigenous populations across the Americas, and a pathogen that depends on sustained human-to-human contact loses lineages when its host communities collapse. Colonisation also introduced new movement of people, and with them new opportunities for a strain to expand across a continent.
The study does not claim to have resolved which of those mechanisms operated. What it establishes is that the modern distribution of M. lepromatosis is not a direct readout of the ancient one — an important caution, since inferring deep history from present-day pathogen diversity is exactly the reasoning this work was needed to correct.
The species' non-human hosts add a further complication. M. lepromatosis has been found in red squirrels in the British Isles, and M. leprae in armadillos in the Americas. Animal reservoirs mean a pathogen's history is not only a human one, and that host jumps in either direction are part of the picture that ancient genomes are only beginning to resolve.
Limitations#
| Limitation | Why it matters |
|---|---|
| Two ancient genomes | Establishes presence on two continents, not prevalence anywhere. |
| Ancient pathogen DNA is fragmentary | Reconstructed genomes may be incomplete relative to the living strain. |
| Screening coverage is uneven | Where nobody has screened, absence of evidence means very little. |
| Detection is not diagnosis | Bacterial DNA shows infection, not clinical disease or cause of death. |
| Dates carry ranges | "Roughly a thousand years ago" spans radiocarbon intervals, not a year. |
| Modern sampling shapes phylogeny | Present-day clades are resolved from the samples that happen to exist. |
Frequently asked questions about pre-contact leprosy in the Americas#
Which pathogen was found?#
Mycobacterium lepromatosis, a leprosy-causing bacterium described as a distinct species in 2008 and found mainly in the Americas. It is not M. leprae, the pathogen behind most historically documented leprosy.
Where and when did the ancient cases occur?#
Ancient genomes were recovered from individuals in Canada and Argentina, both from pre-contact contexts dating to roughly a thousand years ago.
How many samples were tested?#
The team screened 389 ancient and 408 contemporary samples, substantially expanding the genetic data available for the species.
Does this mean Europeans did not bring disease to the Americas?#
No. The catastrophic epidemics that followed 1492 were caused by acute infectious diseases such as smallpox and measles, and that history is unchanged. This study concerns one chronic infection that was already present.
Was leprosy widespread in the pre-contact Americas?#
The close genetic relationship between strains from Canada and Argentina suggests the bacterium may have been widespread during the Late Holocene, but two ancient genomes cannot establish how many people were infected.
Does leprosy still occur in the Americas?#
Yes. Leprosy remains present in several countries, including cases caused by M. lepromatosis, and it is curable with multidrug therapy. This study is about the disease's deep history and has no bearing on current diagnosis or treatment.
Testing instead of assuming#
The core of this result is methodological. The claim that leprosy arrived in the Americas with Europeans was never based on a negative test; it was based on the absence of a positive one, in a period when the relevant pathogen had not been described and nobody was screening for it.
Once someone screened — nearly eight hundred samples, ancient and modern — the answer changed. A second leprosy bacterium was already there, in individuals separated by the length of two continents, carrying strains close enough to imply real circulation.
The wider point is that the ancient disease record is still mostly untested, and its shape reflects where research effort has gone rather than where pathogens were. Every large screening programme in a region that has not had one is a candidate to rewrite a chapter of this kind — which is a good reason to treat the current map of ancient disease as provisional rather than settled.
Sources and further reading#
- Lopopolo, M., Avanzi, C., Duchene, S. et al. (2025). Pre-European contact leprosy in the Americas and its current persistence. Science 389, eadu7144. DOI: 10.1126/science.adu7144.
- Institut Pasteur, Microbial Paleogenomics Unit: research.pasteur.fr.
- Han, X. Y., Seo, Y.-H., Sizer, K. C. et al. (2008). A new Mycobacterium species causing diffuse lepromatous leprosy. American Journal of Clinical Pathology 130, 856–864 — the original species description.
Editorial note: this article was written as a source-based synthesis and distinguishes pathogen detection from clinical diagnosis and prevalence throughout. Its hero and section artwork was generated with AI as an interpretive archaeological scene, not as scientific evidence, and does not depict illness.
